Abstract

To determine the effects of 16 weeks of resistive training alone (RT) and with weight loss (RT+WL) on insulin action, plasma leptin concentrations and leptin's relationship to beta-cell sensitivity to glucose, resting metabolic rate (RMR), and plasma catecholamines in older women. Fifteen obese postmenopausal women aged 50-69 y. Body composition (by dual-energy X-ray absorptiometry), RMR (by indirect calorimetry), insulin action (by 2 h hyperglycemic clamps; 7.9 mmol/l above basal plasma glucose levels), plasma leptin and insulin (by RIA), and plasma catecholamines (by enzymatic methods). RT and RT+WL resulted in significant improvements in muscular strength (P<0.01) with no changes in maximal oxygen consumption. Body weight, fat mass and percent body fat did not change with RT, but decreased with RT+WL (P<0.001). Fat-free mass and RMR increased after training when both groups were combined (P<0.05). The insulin response during the last 20 min of the 2 h hyperglycemic clamps decreased 16% after RT (P=0.05), 43% after RT+WL (P<0.05), and 29% in the entire group (P<0. 01) without any changes in glucose utilization. Plasma leptin levels did not change after RT, but decreased by 36% after RT+WL (P<0.05). Baseline leptin levels correlated with body weight (r=0.68, P<0.01), body fat mass (r=0.77, P<0.001), and RMR (kcal/d; (r=0.69, P<0.005), but not with baseline norepinephrine or epinephrine levels. Plasma leptin levels correlated with basal insulin (r=0.73, P<0.005), and approached significance with the 0-10 min and 100-120 min insulin response to hyperglycemia before training (both r=0.51, P=0.07). In the entire group, the change in insulin response from 100-120 min during the clamp correlated with the change in leptin levels (r=0.60, P<0.05), but this was not independent of changes in fat mass. Although changes in leptin levels were not related to changes in RMR or plasma catecholamines after RT with and without weight loss, the increase in insulin action after training and weight loss may be related to the decrease in leptin levels that were mediated by the loss of body fat in the obese, postmenopausal women. International Journal of Obesity (2000)24, 27-32

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